Proteomics investigation reveals apoptosis-associated proteins in aryl hydrocarbon receptor-deficient human lung cells treated with 2,3,7,8-Tetrachlorobenzo-p-Dioxin

[[abstract]]2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the most potent dioxin, binds to aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, which subsequently alters gene expression. Epidemiological studies suggested that exposure to TCDD highly enhanced the risk of pulmonary diseases. In this study, we adopted a comparative proteomic approach using two-dimensional gel electrophoresis (2DE) to identify the differential expression of proteins between TCDD-treated control and AhR-deficient lung adenocarcinoma cells. Fifteen proteins from seventeen differential protein spots were identified that four of which were down-regulated and eleven were up-regulated. Western blotting analysis confirmed differential expression for five identified proteins, including GRB10, YWHAG, HSP27, LGALS1 and ACTB. Further protein-protein interaction network analysis of the identified proteins illustrated that twelve proteins were linked to a network containing caspase-3, p53, MDM2 and Akt/PKB, which is known to be associated with apoptosis pathway. Among the identified proteins, GRB10 may play a critical role to regulate the development of apoptosis in human lung cells by TCDD exposure. According to our study, it is expected to lead to new insights into the apoptosis pathway in lung adenocarcinoma by TCDD exposure